CLDN11

(redirected from claudin-11)

CLDN11

A gene on chromosome 3q26.2-q26.3 that encodes claudin-11, an integral membrane protein of the claudin family, the members of which form a physical barrier that prevents solutes and water from passing freely into the interstitial space between epithelial or endothelial cell sheets, and play critical roles in maintaining cell polarity and signal transduction. Claudin-11 is a major component of CNS myelin and plays a key role in regulating proliferation and migration of oligodendrocytes.
References in periodicals archive ?
Background: Claudin-5, claudin-9, and claudin-11 are expressed in endothelial cells to constitute tight junctions, and their deficiency may lead to hyperpermeability, which is the initiating process and pathological basis of cardiovascular disease.
sup][10],[11] Claudin-9 and claudin-11 have also been reported to be expressed in endothelial cells, and function as important tight junction proteins.
sup][21],[22],[23] Although TXL has been reported to have positive effects on the hypoxia-inhibited claudin-1,[sup][24],[25] whether TXL regulates claudin-5, claudin-9, and claudin-11, which are expressed in the endothelial cells, has not been explored.
To investigate whether TXL modulate claudin-9 and attenuate cell injury in hypoxia, the cells were exposed to hypoxia and treated with TXL and then the messenger RNA (mRNA) expression of claudin-5, claudin-9, and claudin-11 was examined by real-time reverse transcription-polymerase chain reaction (RT-PCR), the claudin-9 protein content was evaluated by western blotting, the claudin-9 distribution was evaluated by immunofluorescence, and cell morphological changes were observed in light microscope.
After the hypoxia-stimulated cells were treated with TXL for 24 h, the mRNA expression of claudin-5, claudin-9, and claudin-11 was measured.
First, we analyzed claudins by the BioGPS and found that claudin-5, claudin-9, and claudin-11 are highly expressed in the heart.
Claudin-5, claudin-9, and claudin-11 are expressed in endothelial cells to constitute tight junctions, and their deficiency may lead to endothelial hyperpermeability, which is considered as the initiating process and pathological basis of cardiovascular disease.
sup][7],[8],[9] We analyzed and found that claudin-5, claudin-9, and claudin-11 are highly expressed in the heart, and they have all been reported to be expressed in endothelial cells.
The results demonstrated that hypoxia dramatically suppressed claudin-9 expression, without a notable effect onclaudin-5 and claudin-11.